Preβ1-HDL binds to TG-rich lipoproteins and its release is impaired in the postprandial state among patients with poorly controlled type 2 diabetes.

Background: Although preβ1-high-density lipoprotein (preβ1-HDL) promotes cholesterol efflux, high fasting preβ1-HDL levels after breakfast are reduced in patients with poorly controlled type 2 diabetes.

Objective: This study investigated whether preβ1-HDL binds to triglyceride (TG)-rich lipoproteins (TGRLs) in the postprandial state and is released during lipolysis.

Methods: We measured preβ1-HDL concentrations, lecithin-cholesterol acyltransferase (LCAT) activity, and LCAT-dependent preβ1-HDL conversion before and after breakfast in patients with diabetes. We also performed in vitro studies using TGRLs. Preβ1-HDL was quantified by enzyme-linked immunosorbent assay and native two-dimensional gradient gel (N-2D-gel) electrophoresis.

Results: Before breakfast, the diabetes group had higher preβ1-HDL concentrations than the healthy controls; after breakfast, levels in the two groups were similar. Neither LCAT mass nor the LCAT-dependent preβ1-HDL conversion rate changed after breakfast. Mixing of fasting plasma with chylomicrons or very-low-density lipoprotein (VLDL) reduced the preβ1-HDL level by 15% ± 4% and 45% ± 10%, respectively. N-2D-gel electrophoresis showed that preβ1-HDL was generated by bacteria-derived TG lipase only from postprandial VLDL of patients with type 2 diabetes.

Conclusion: Preβ1-HDL binds to TGRLs in the postprandial state and is released during lipolysis, implying that postprandial hyperlipidemia impairs reverse cholesterol transport in patients with poorly controlled type 2 diabetes.